Introduction: Hepatocellular carcinoma (HCC) is the most common and prevalent cancer type among liver cancers. In this study, expression of miR-490-3p and aurora kinase A gene (AURKA) was investigated in HCC. Additionally, we explored the microRNA (miR)-490-3p/AURKA relationship as well as the influence on HCC cell proliferation and migration. Material and methods: The dual luciferase reporter assay serves to verify the target relationship between miR-490-3p and AURKA. miR-490-3p mimics, AURKA siRNA and AURKA cDNA, were transfected into HCC cells. Quantitative real-time polymerase chain reaction and western blot were chosen for examining the relative expression of miR-490-3p and AURKA in HCC tissues, adjacent tissues, HCC cells and normal cells. The study detected the proliferation of HCC cells with the application of MTT assay and colony formation assay. Transwell assay was applied for the observation of migration, and wound healing assay for invasion. Results: The experiment results showed that miR-490-3p expression was down-regulated and AURKA expression was up-regulated in HCC cells and tissues. AURKA was the target gene of miR-490-3p and overexpression of miR-490-3p could inhibit the expression of AURKA in HCC cells. miR-490-3p overexpression could inhibit HCC cell migration and invasion, while AURKA promoted HCC cell migration. All experiment results indicated that miR-490-3p was low-expressed while AURKA was over-expressed in HCC cells and tissues compared to normal liver cells and tissues. Conclusions: miR-490-3p could down-regulate the expression of AURKA, thus suppressing the proliferation and migration of HCC cells.
BackgroundThe objective of this study was to explore the role of SIX1 in paclitaxel (TAX) resistance of HepG2 cells via reactive oxygen species (ROS) and autophagy pathway.Material/MethodsHepatoma cell line HepG2 was treated with SIX1 knockdown or/and TAX. Cell growth was detected by MTT assay and colony formation assay. Cell apoptosis was evaluated with flow cytometry. ROS levels were detected using flow cytometry (stained with DCFH2-DA). Western blot was conducted to detect the expression of SIX1 and autophagy-related proteins.ResultsTAX suppressed the proliferation of HepG2 cells in a time/dose-dependent manner, and upregulated the expression of SIX1. SIX1 siRNA increased TAX sensitivity of HepG2 cells and upregulated cell ROS levels. SIX1 siRNA combined with TAX treatment activated autophagy of HepG2 cells. N-acetyl-L-cysteine (NAC) partially attenuated SIX1 siRNA-induced ROS level increases, and autophagy inhibitor 3-MA notably enhanced SIX1 siRNA-induced cell apoptosis.ConclusionsKnockdown of SIX1 increased cell ROS levels and autophagy, promoted cell apoptosis, and enhanced TAX sensitivity of HepG2 cells.
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